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Monday November 09 2009 | Biotechnology feed | All feeds
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HSP90 modulated VR1 function Acute pain resulting from conditions such as headache, muscle spasms, dental problems or following surgery affects 90 million people per year in the US alone. Chronic pain affects a further 40-70 million and is more troubling as it sparks a viscous cycle of clinical problems and often precipitates depression and/or life-style changes. Furthermore, establishing prolonged analgesia free of serious side effects is a particularly challenging area of medicine. The total economic cost of pain is US$100 billion and global sales of analgesics and anti-inflammatories has been estimated as US$18.7 billion worldwide. Analgesia is currently treated by NSAIDs or by opiates. The former is related to well publicized and serious GI problems while the latter causes unwanted side central side effects. New analgesics are therefore urgently required (see our recent feature "Future Pain Drugs" for a full analysis of this field). Capsaicin and other similar molecules such as resiniferatoxin have been targeted as therapeutic approaches to analgesia, however this field took a major step forward in 1997 following the identification of the vanilloid receptor VR1 and more recently other member of this receptor family. Consequent advances in vanilloid pharmacology are now starting to produce therapeutic candidates and indeed the number of vanilloid ligands in pharmaceutical development has doubled over the past year. Researchers Brigham and Women's Hospital, Harvard Medical School, have been investigating the role that heat shock proteins (HSPs) play in pain pathways. This group reports that the HSP90 inhibitor, geldanamycin, alters capsaicin stimulated currents in DRG cells. HSP90 has recently been implicated in inflammation and the present study therefore suggests that targeting the interaction between VR1 and HSP90 may modulate inflammatory hyperalgesia. Entry date October, 2002 Adapted from McDowell & Yukhananov, Neuroreport 2002 Mar 25;13(4):437-41
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